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FUT1-mediated terminal fucosylation acts as a new target to attenuate renal fibrosis
Jialiang Luo1, Kaifeng Mao2, Zhengyumeng Zhu3
1Department of Dermatology, the Fifth Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, 510900, China. 1592949558@qq.com.
Backgrounds:
Renal fibrosis is a common pathologic process of most chronic kidney diseases (CKDs), becoming one of the major public health problems worldwide. Terminal fucosylation plays an important role in physiological homeostasis and pathological development. The present study aimed to explore the role of terminal fucosylation during kidney fibrogenesis and propose a possible anti-fibrosis treatment via suppressing aberrant terminal fucosylation.
Methods:
We investigated the expression level of fucosyltransferase1 (FUT1) in CKD patients by using public database. Then, we further confirmed the level of terminal fucosylation by UEA-I staining and FUT1 expression in unilateral ureteral obstruction (UUO)-induced renal fibrosis mice. Immunostaining, qPCR, western blotting and wound healing assay were applied to reveal the effect of FUT1 overexpression in human kidney proximal tubular epithelial cell (HK-2). What's more, we applied terminal fucosylation inhibitor, 2-Deoxy-D-galactose (2-D-gal), to determine whether suppressing terminal fucosylation ameliorates renal fibrosis progression in vitro and in vivo.
Results:
Here, we found that the expression of FUT1 significantly increased during renal fibrosis. In vitro experiments showed upregulation of epithelial-mesenchymal transition (EMT) after over-expression of FUT1 in HK-2. Furthermore, in vivo and in vitro experiments indicated that suppression of terminal fucosylation, especially on TGF-βR I and II, could alleviate fibrogenesis via inhibiting transforming growth factor-β (TGF-β)/Smad signaling.
Conclusions:
The development of kidney fibrosis is attributed to FUT1-mediated terminal fucosylation, shedding light on the inhibition of terminal fucosylation as a potential therapeutic treatment against renal fibrosis.
Insights
Terminal fucosylation, driven by fucosyltransferase 1 (FUT1), promotes kidney fibrosis. Inhibiting this process offers a potential therapeutic strategy for chronic kidney diseases.
Area of Science:
- Nephrology
- Glycobiology
- Pathology
Background:
- Renal fibrosis is a hallmark of chronic kidney diseases (CKDs) and a significant global health concern.
- Terminal fucosylation is implicated in both normal physiological processes and disease development.
Purpose of the Study:
- To investigate the role of terminal fucosylation in kidney fibrogenesis.
- To explore the potential of suppressing terminal fucosylation as an anti-fibrosis treatment.
Main Methods:
- Analyzed fucosyltransferase 1 (FUT1) expression in CKD patients and a mouse model of renal fibrosis.
- Utilized UEA-I staining, qPCR, western blotting, and wound healing assays.
- Investigated the effects of a terminal fucosylation inhibitor (2-Deoxy-D-galactose) in vitro and in vivo.
Main Results:
- FUT1 expression was significantly elevated in renal fibrosis.
- Overexpression of FUT1 induced epithelial-mesenchymal transition (EMT) in kidney cells.
- Inhibition of terminal fucosylation ameliorated fibrosis by suppressing TGF-β/Smad signaling.
Conclusions:
- FUT1-mediated terminal fucosylation contributes to kidney fibrosis development.
- Targeting terminal fucosylation presents a promising therapeutic avenue for renal fibrosis.
